The lung has its own local host defense mechanism designed to protect this vital organ from exposure to injury, inflammatory conditions and microbiological agents, both from the inhaled route and from blood circulation. This local host defense mechanism is dependent on endogenous expression of granulocyte macrophage colony stimulating factor (GM-CSF) by the alveolar cells in the alveolar and peripheral airways. This local mechanism is isolated from the systemic circulation since GM-CSF does not pass from the airspaces to the circulation and vice versa. Thus, expression of GM-CSF in the lung does not increase circulating monocytes and neutrophils in the circulation and no functional effects are seen in the lung upon systemic administration of GM-CSF. This is due to the fact that the GM-CSF molecule is too big to traverse the transalveolar-capillary passage. Further GM-CSF molecule is a water-soluble molecule. Without endogenous GM-CSF expression, the resting macrophages of the lung are not activated into the highly immune competent dendritic alveolar cells which orchestrate the lung's local defense mechanism.